Platelets, when exposed to proper agonists, undergo several responses which appear to be contractile in nature. We have found the platelet myosin is phosphorylated in response to such agonists. Our studies involve correlation of platelet function with platelet myosin phosphorylation in order that the role of platelet contractile proteins in these functions might be discerned. Platelet function depends on a continuous supply of ATP. It is unclear whether ATP is used to keep platelets responsive and/or to drive these functions. We recently found that ADP bound to actin is rapidly turning over, possibly resulting in a continuous consumption of ATP amounting to 40% of the total. Preliminary studies indicate that the ADP-ATP turnover is reduced after platelet excution of hemostatic functions. We want to correlate this turnover rate to action filament formation in platelets. We are investigating the hypothesis that the state of actin determines the responsiveness of platelets.